This is a study to establish a definitive role for calcitonin in mammalian physiology. It is based on the postulate that this role is central to the most optimum control of calcium homeostasis during the postpradial period. The overall postulate places calcitonin as a key hormone in directing calcium from the intestines into bone. To do this, it influences both the percentage of oral intake of calcium that reaches bone, and its locations in bone. Rats trained to consume their daily food allotment (16 g) in 2 hours will be studied during subsequent postprandial periods. The four groups will be : 1) Thyroid-intact, vitamin D replete(TI(+)D); 2) Thyroid-intact vitamin D deficient (TI(-)D); 3) Thyroidectomized, vitamin D replete (TX(+)D); and 4) Thyroidectomized, vitamin D deficient (TX(-)D). All rats will have transplanted parathyroid glands; and throidectomized rats will receive T4 (0.02 ug/g) 4 times weekly. The primary data obtained will be for plasma levels of calcitonin, parathyroid hormone, and 1,25(OH)2D3 and relative rates of intestinal calcium absorption. All data will be related to specific time intervals after feeding. The first study will be in rate maintained on a constant daily intake of calcium (95 mg). This will be followed by a study of the effect of: a) a shift in the daily intake of calcium to 160 mg; and b) postpradial injection of calcitonin and/or parathyroid hormone to TX rate. The major premise of this study is that calcitonin, present postprandially, indirectly modulates secretion of parathyroid hormone: formation of 1,25(HO)2D3; and rates of intestinal absorption of calcium. By so doing, calcitonin maximizes calcium transfer from the intestines to bone, while minimizing daily fluctuations in plasma levels of the other hormes. Preliminary clinical studies by Dr. Grubb of our department indicate that these postprandial controls are present in humans.